Diffusivity and quantitative T1 profile of human visual white matter tracts after retinal ganglion cell damage
Diffusivity and quantitative T1 profile of human visual white matter tracts after retinal ganglion cell damage
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DOI：
10.1016/j.nicl.2019.101826
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发表时间：
2019-01-01
影响因子：
4.2
通讯作者：
Masuda, Yoichiro
中科院分区：
文献类型：
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作者：
Takemura, Hiromasa;Ogawa, Shumpei;Masuda, Yoichiro
在患有视网膜神经节细胞疾病的患者中，最近的扩散张量成像（DTI）研究揭示了视觉白色物质束（例如视束）和视辐射的结构异常。然而，这些扩散率变化的微观结构起源是未知的，因为DTI指标涉及多种生物因素，并且与特定的微观结构特性不直接相关。相比之下，最近的定量T1（qT1）映射方法提供的组织特性测量相对特定的髓鞘体积分数在白色的问题。本研究旨在通过结合DTI和qT1测量，提高我们对Leber遗传性视神经病变（LHON）患者视网膜神经节细胞损伤后视觉白色物质束微结构变化的理解。我们收集了7名LHON患者和20名年龄匹配的对照受试者的这些测量结果。对于所有的人，我们确定了视束和视辐射使用概率纤维束成像，并评估扩散率和qT1曲线沿着他们。LHON患者和对照组的视束扩散率和qT1测量值差异显著。在光学辐射，这些变化中观察到的扩散率，但不明显的qT1测量。这表明，髓磷脂损失可能无法解释作为视网膜神经节细胞疾病的结果的视辐射的跨突触扩散率的变化。
In patients with retinal ganglion cell diseases, recent diffusion tensor imaging (DTI) studies have revealed structural abnormalities in visual white matter tracts such as the optic tract, and optic radiation. However, the microstructural origin of these diffusivity changes is unknown as DTI metrics involve multiple biological factors and do not correlate directly with specific microstructural properties. In contrast, recent quantitative T1 (qT1) mapping methods provide tissue property measurements relatively specific to myelin volume fractions in white matter. This study aims to improve our understanding of microstructural changes in visual white matter tracts following retinal ganglion cell damage in Leber's hereditary optic neuropathy (LHON) patients by combining DTI and qT1 measurements. We collected these measurements from seven LHON patients and twenty age-matched control subjects. For all individuals, we identified the optic tract and the optic radiation using probabilistic tractography, and evaluated diffusivity and qT1 profiles along them. Both diffusivity and qT1 measurements in the optic tract differed significantly between LHON patients and controls. In the optic radiation, these changes were observed in diffusivity but were not evident in qT1 measurements. This suggests that myelin loss may not explain trans-synaptic diffusivity changes in the optic radiation as a consequence of retinal ganglion cell disease.